A5091539906- Parkinson's Disease Mechanisms and Treatments
- Alzheimer's disease research and treatments
- Neurological diseases and metabolism
- Neurological disorders and treatments
- Traumatic Brain Injury and Neurovascular Disturbances
- Prion Diseases and Protein Misfolding
- Intracranial Aneurysms: Treatment and Complications
- Nerve injury and regeneration
- Neurosurgical Procedures and Complications
- Nuclear Receptors and Signaling
- Neuroscience and Neuropharmacology Research
- Neuroinflammation and Neurodegeneration Mechanisms
- S100 Proteins and Annexins
- Neuroscience and Neural Engineering
- Electron Spin Resonance Studies
- Botulinum Toxin and Related Neurological Disorders
- Amino Acid Enzymes and Metabolism
- Migraine and Headache Studies
- Vascular Malformations Diagnosis and Treatment
- Genetic Neurodegenerative Diseases
- DNA and Nucleic Acid Chemistry
- Autophagy in Disease and Therapy
- Inflammatory mediators and NSAID effects
- Cholinesterase and Neurodegenerative Diseases
- Traumatic Ocular and Foreign Body Injuries
Florida College
2020-2025
University of Florida
2016-2025
Case Western Reserve University
2022
Abstract Tau protein abnormally aggregates in tauopathies, a diverse group of neurologic diseases that includes Alzheimer’s disease (AD). In early stages disease, tau becomes hyperphosphorylated and mislocalized, which can contribute to its aggregation toxicity. We demonstrate phosphorylation at Ser208 (pSer208) promotes microtubule dysfunction cultured cells. Comparative assessment the epitopes recognized by antibodies AT8, CP13, 7F2 demonstrates CP13 are specific for Ser202 Thr205,...
Abstract Pathology consisting of intracellular aggregates alpha-Synuclein (α-Syn) spread through the nervous system in a variety neurodegenerative disorders including Parkinson’s disease, dementia with Lewy bodies, and multiple atrophy. The discovery structurally distinct α-Syn polymorphs, so-called strains, supports hypothesis where strain-specific structures are templated into formed by native α-Syn. These strains hypothesised to dictate spreading pathology tissue cellular impact...
Misfolded α-synuclein (αS) is hypothesized to spread throughout the central nervous system (CNS) by neuronal connectivity leading widespread pathology. Increasing evidence indicates that it also has potential invade CNS via peripheral nerves in a prion-like manner. On basis of effectiveness following routes prion administration, we extend our previous studies neuroinvasion M83 αS transgenic mice hind limb muscle (intramuscular [i.m.]) injection fibrils comparing various sites inoculations...
The protein α-synuclein (αsyn) forms pathologic aggregates in a number of neurodegenerative diseases including Lewy body dementia (LBD) and Parkinson's disease (PD). It is unclear why such as LBD may develop widespread αsyn pathology, while Alzheimer's with amygdala restricted bodies (AD/ALB) the remain localized. contains both AD/ALB; to understand pathology continues progress but not AD/ALB, tissue from other regions were obtained 14 cases LBD, 9 4 controls for immunohistochemical...
Prionoid transmission of α-synuclein (αSyn) aggregates along neuroanatomically connected projections is posited to underlie disease progression in α-synucleinopathies. Here, we specifically wanted study whether this prionoid occurs via direct inter-neuronal transfer and, if so, would intrastriatal injection αSyn lead nigral degeneration.To test the nigro-striatal pathway, injected amyloidogenic into two different regions striatum adult human wild type transgenic mice (Line M20) or...
Traumatic dural arteriovenous fistula (dAVF) formation rarely occurs following calvarial fractures. dAVFs, if untreated, may rupture, causing devastating intracranial hemorrhage, and the presence of cortical venous drainage increases risk rupture mortality. A female in her sixth decade life developed a traumatic dAVF middle meningeal artery (MMA) after being hit by motor vehicle. The MMA drained into superior petrosal sinus vein Labbe consistent with Cognard grade 3 lesion. This was...
In synucleinopathies, including Parkinson's disease (PD), dopamine neurons in the substantia nigra pars compacta (SNc) exhibit greater vulnerability to degeneration than those ventral tegmental area (VTA). While α-synuclein (αSyn) pathology is implicated nigral neuron loss, mechanisms by which αSyn affects neuronal activity and midbrain network connectivity prior cell death remain unclear. This study tested hypothesis that elevated expression induces pathophysiological changes firing...
The accumulation of alpha-synuclein (αS) inclusions is a hallmark feature Parkinson's disease (PD) and PD-related diseases. Recently, number studies have demonstrated similarities between the prion protein αS, including its ability to spread along neuroanatomical tracts throughout central nervous system (CNS). However, there are caveats in each these which injection routes used had potential result widespread dissemination αS-containing inocula, making it difficult precisely define...
Abstract Co-occurrence of tau and α-synuclein pathologies in a subset Alzheimer’s disease patients has led to the idea that mixed may play unique characteristic role neurodegenerative cascade. To understand aetiology such pathologies, we investigated cross-seeding by human recombinant fibrillar species mouse model tauopathy (Line PS19) or synucleinopathy M20). Unilateral hippocampal injection fibrils fibrils, lesser extent + copolymer prepared from co-incubating individual monomers, induced...
α-synuclein (αS) is an abundant, neuronal protein that assembles into fibrillar pathological inclusions in a spectrum of neurodegenerative diseases include Lewy body (LBD) and Multiple System Atrophy (MSA). The cellular regional distributions vary widely between different synucleinopathies contributing to the clinical presentations. Extensive cleavage within carboxy (C)-terminal region αS associated with inclusion formation, although events leading these modifications implications for...
Abstract Synucleinopathies, including Parkinson’s disease (PD), Lewy body dementia (LBD), Alzheimer’s with amygdala restricted bodies (AD/ALB), and multiple system atrophy (MSA) comprise a spectrum of neurodegenerative disorders characterized by the presence distinct pathological α-synuclein (αSyn) inclusions. Experimental studies support notion that αSyn aggregates contribute to cellular demise dysfunction progression associated prion-like spread via conformational templating. The...
Pathophysiological damages and loss of function dopamine neurons precede their demise contribute to the early phases Parkinson's disease. The presence aberrant intracellular pathological inclusions protein α-synuclein within ventral midbrain dopaminergic is one cardinal features We employed molecular biology, electrophysiology, live-cell imaging investigate how excessive expression alters multiple characteristics neuronal dynamics transmission in cultured conditionally expressing GCaMP6f....
Background A clinical hallmark of aneurysmal SAH (aSAH) is headache. Little known about post-aSAH headache factors which may point to underlying mechanisms. In this study, we aimed characterize the severity and trajectory headaches in relation features patients with aSAH.Methods This a retrospective longitudinal study adult admitted an academic tertiary care center between 2012 2019 aSAH who could verbalize pain scores. Factors recorded included demographics, aneurysm characteristics,...